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This paper suggests potentially important additional insight into a mechanism by which Aβ is related to synaptic toxicity. The indication of an effect on synaptic vesicles is consistent with data on deficits in molecules related to vesicle trafficking in AD. The ultimate proof of the relevance to AD of the mechanism proposed would be a quantitative electron microscopic evaluation of synaptic vesicles in postmortem human material. This would require exceptionally well-preserved material.

Recent studies have revealed detrimental effects of soluble Aβ aggregates on plasticity-related receptors located in the post-synaptic terminal. The current study adds an interesting new perspective on possible early actions of soluble Aβ aggregates on mechanisms controlling presynaptic vesicle release. It may, thus, be that the initial impact of Aβ includes both pre- and post-synaptic mechanisms underlying synaptic function.